Chronic inflammation increases the sensitivity of mouse Treg for TNFR2 costimulation
Zitieren Sie bitte immer diese URN: urn:nbn:de:bvb:20-opus-173259
- TNF receptor type 2 (TNFR2) has gained attention as a costimulatory receptor for T cells and as critical factor for the development of regulatory T cells (Treg) and myeloid suppressor cells. Using the TNFR2-specific agonist TNCscTNF80, direct effects of TNFR2 activation on myeloid cells and T cells were investigated in mice. \(In\) \(vitro\), TNCscTNF80 induced T cell proliferation in a costimulatory fashion, and also supported \(in\) \(vitro\) expansion of Treg cells. In addition, activation of TNFR2 retarded differentiation of boneTNF receptor type 2 (TNFR2) has gained attention as a costimulatory receptor for T cells and as critical factor for the development of regulatory T cells (Treg) and myeloid suppressor cells. Using the TNFR2-specific agonist TNCscTNF80, direct effects of TNFR2 activation on myeloid cells and T cells were investigated in mice. \(In\) \(vitro\), TNCscTNF80 induced T cell proliferation in a costimulatory fashion, and also supported \(in\) \(vitro\) expansion of Treg cells. In addition, activation of TNFR2 retarded differentiation of bone marrow-derived immature myeloid cells in culture and reduced their suppressor function. \(In\) \(vivo\) application of TNCscTNF80-induced mild myelopoiesis in naïve mice without affecting the immune cell composition. Already a single application expanded Treg cells and improved suppression of CD4 T cells in mice with chronic inflammation. By contrast, multiple applications of the TNFR2 agonist were required to expand Treg cells in naïve mice. Improved suppression of T cell proliferation depended on expression of TNFR2 by T cells in mice repeatedly treated with TNCscTNF80, without a major contribution of TNFR2 on myeloid cells. Thus, TNFR2 activation on T cells in naïve mice can lead to immune suppression \(in\) \(vivo\). These findings support the important role of TNFR2 for Treg cells in immune regulation.…
Autor(en): | Tobias Schmid, Lena Falter, Sabine Weber, Nils Müller, Konstantin Molitor, David Zeller, Dorothea Weber-Steffens, Thomas Hehlgans, Harald Wajant, Sven Mostböck, Daniela N. Männel |
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URN: | urn:nbn:de:bvb:20-opus-173259 |
Dokumentart: | Artikel / Aufsatz in einer Zeitschrift |
Institute der Universität: | Medizinische Fakultät / Abteilung für Molekulare Innere Medizin (in der Medizinischen Klinik und Poliklinik II) |
Sprache der Veröffentlichung: | Englisch |
Titel des übergeordneten Werkes / der Zeitschrift (Englisch): | Frontiers in Immunology |
Erscheinungsjahr: | 2017 |
Band / Jahrgang: | 8 |
Aufsatznummer: | 1471 |
Originalveröffentlichung / Quelle: | Frontiers in Immunology (2017) 8:1471. https://doi.org/10.3389/fimmu.2017.01471 |
DOI: | https://doi.org/10.3389/fimmu.2017.01471 |
PubMed-ID: | https://pubmed.ncbi.nlm.nih.gov/29163535 |
Allgemeine fachliche Zuordnung (DDC-Klassifikation): | 6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit |
Freie Schlagwort(e): | MDSC; TNFR2; costimulation; immune regulation; inflammation; molecular medicine; regulatory T cell |
Datum der Freischaltung: | 24.06.2021 |
Lizenz (Deutsch): | CC BY: Creative-Commons-Lizenz: Namensnennung 4.0 International |